The present invention relates generally to a method of treating a surface to impart a controlled hydrophobic character; and more particularly to a method of treating a surface with a silicon-containing compound to control the hydrophobicity of the surface and to reduce the adsorption of protein.
"Siliconization" is defined to be the imparting of silicone-like properties to a substrate material by addition or reaction of silicon containing compounds with the substrate resulting in the formation of a thin surface film. At times siliconization is used merely to obtain a hydrophobic surface. However, often the objective of siliconization is to prevent undesired interaction between the surface and biological macromolecules. While the biocompatibility of silicone elastomers has been well examined, siliconized substrate materials demonstrate a broader range of bio-interaction.
Although materials intended for applications such as implants and invasive and extracorporeal support devices have been well studied, materials which have "ex vivo" contact with biological tissues have been largely ignored. While substrate siliconization is employed in a variety of analytical techniques, and glass contacting surfaces are often siliconized, blood contact with glass has been generally overlooked. Siliconized surfaces in general exhibit a low level of interaction with "blood fluids," which are defined to include whole blood, components thereof, and products prepared therefrom including blood fractions, and other protein-containing fluids, yet that interaction may be critical for subsequent diagnostic analysis of blood fluids and other protein-containing fluids stored in glass. As a rule, accurate diagnostic tests require minimal interaction between the glass storage or transfer vessel and the blood fluid.
The interaction of blood with foreign surfaces such as the walls of storage containers or the surfaces of implants, in the absence of inhibitors, is a rapid series of events sensitive to a variety of factors. Foreign surfaces ideally should resemble vascular endothelia which provide a nonthrombogenic surface resistant to platelet adhesion and aggregation. However, biomaterials generally present non-ideal surfaces. Consequently, exposure to the biomaterial surface may trigger a thrombogenic cascade in the blood. Plasma proteins are adsorbed and platelets and leukocytes adhere to the surface. Platelets are activated by a release reaction and recruitment of nearby platelets with the eventual formation of the thrombus. Subsequently, formation of crosslinked fibrin stabilizes the thrombus. In addition, complement activation may occur mediating a long term immunological response to the surface.
Another important factor is the tendency of some surfaces to lyse erythrocytes. While erythrocytes represent only 40 percent of blood in terms of packed cell volume, erythrocytes contain 140 milligrams hemoglobin protein per milliliter whole blood, and less than 0.01 mg/ml of hemoglobin is found in the plasma. Thus, a biomaterial surface which causes hemolysis raises the level of free blood protein and effects a profound change in blood characteristics.
An ideal biomaterial surface would not activate the thrombogenic cascade, the complement system, or cause hemolysis. Because protein adsorption is important in initiating the thromobogenic cascade and in complement activation, and because minimal interaction of blood fluid with the containers in which it is stored is generally desirable for diagnostic test accuracy, there is a clear need for a siliconization technique which minimizes adsorption of protein from blood fluids.